scholarly journals Actomyosin controls planarity and folding of epithelia in response to compression

2018 ◽  
Author(s):  
Tom P. J. Wyatt ◽  
Jonathan Fouchard ◽  
Ana Lisica ◽  
Nargess Khalilgharibi ◽  
Buzz Baum ◽  
...  

ABSTRACTThroughout embryonic development and adult life, epithelia are subjected to external forces. The resulting deformations can have a profound impact on tissue development and function. These include compressive deformations which, although hard to study in model systems due to the confounding effects of the substrate, are thought to play an important role in tissue morphogenesis by inducing tissue folding and by triggering mechanosensitive responses including cell extrusion and cell differentiation. Here, using suspended epithelia, we are able to uncover the immediate response of epithelial tissues to the application of large (5-80%) in-plane compressive strains. We show that fast compression induces tissue buckling followed by active tissue flattening which erases the buckle within tens of seconds. Strikingly, there is a well-defined limit to this second response, so that stable folds form in the tissue for compressive strains larger than ∼35%. Finally, a combination of experiment and modelling shows that the response to compression is orchestrated by the automatic adaptation of the actomyosin cytoskeleton as it re-establishes tension in compressed tissues. Thus, tissue pre-tension allows epithelia to both buffer against fast compression and regulate folding.

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 788 ◽  
Author(s):  
Li ◽  
An ◽  
Zhang

During gametogenesis and early embryonic development, the chromatin architecture changes dramatically, and both the transcriptomic and epigenomic landscape are comprehensively reprogrammed. Understanding these processes is the holy grail in developmental biology and a key step towards evolution. The 3D conformation of chromatin plays a central role in the organization and function of nuclei. Recently, the dynamics of chromatin structures have been profiled in many model and non-model systems, from insects to mammals, resulting in an interesting comparison. In this review, we first introduce the research methods of 3D chromatin structure with low-input material suitable for embryonic study. Then, the dynamics of 3D chromatin architectures during gametogenesis and early embryonic development is summarized and compared between species. Finally, we discuss the possible mechanisms for triggering the formation of genome 3D conformation in early development.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 303-LB
Author(s):  
NAJWA A. AL-JAHDHAMI ◽  
SCOTT J. ANDERSON ◽  
ALI ALDIBBIAT ◽  
JAMES A. SHAW

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sarah J. Brown ◽  
Ibrahim Boussaad ◽  
Javier Jarazo ◽  
Julia C. Fitzgerald ◽  
Paul Antony ◽  
...  

AbstractRecent evidence suggests neurogenesis is on-going throughout life but the relevance of these findings for neurodegenerative disorders such as Parkinson’s disease (PD) is poorly understood. Biallelic PINK1 mutations cause early onset, Mendelian inherited PD. We studied the effect of PINK1 deficiency on adult neurogenesis of dopaminergic (DA) neurons in two complementary model systems. Zebrafish are a widely-used model to study neurogenesis in development and through adulthood. Using EdU analyses and lineage-tracing studies, we first demonstrate that a subset of ascending DA neurons and adjacent local-projecting DA neurons are each generated into adulthood in wild type zebrafish at a rate that decreases with age. Pink1-deficiency impedes DA neurogenesis in these populations, most significantly in early adult life. Pink1 already exerts an early effect on Th1+ progenitor cells rather than on differentiated DA neurons only. In addition, we investigate the effect of PINK1 deficiency in a human isogenic organoid model. Global neuronal differentiation in PINK1-deficient organoids and isogenic controls is similar, but PINK1-deficient organoids display impeded DA neurogenesis. The observation of impaired adult dopaminergic neurogenesis in Pink1 deficiency in two complementing model systems may have significant consequences for future therapeutic approaches in human PD patients with biallelic PINK1 mutations.


2019 ◽  
Vol 29 (4) ◽  
pp. 467-474 ◽  
Author(s):  
Zahra Hoodbhoy ◽  
Nuruddin Mohammed ◽  
Nadeem Aslam ◽  
Urooj Fatima ◽  
Salima Ashiqali ◽  
...  

AbstractObjective:The objective of this study was to assess differences in myocardial systolic and diastolic function and vascular function in children 2−5 years of age born to diabetic as compared to non-diabetic mothers.Methods:This study was a retrospective cohort conducted in 2016 at The Aga Khan University Hospital, Karachi, Pakistan. It included children between 2 and 5 years of age born to mothers with and without exposure to diabetes in utero (n = 68 in each group) and who were appropriate for gestational age. Myocardial morphology and function using echocardiogram and carotid intima media thickness (cIMT) and pulse wave velocity was performed to evaluate cardiac function as well as macrovascular remodelling in these children. Multiple linear regression was used to compare the groups.Results:There was no significant difference in cardiac morphology, myocardial systolic and diastolic function, and macrovascular assessment between the exposed and unexposed groups of AGA children. Subgroup analysis demonstrated a significantly decreased mitral E/A ratio in children whose mothers were on medications as compared to those on dietary control (median [IQR] = 1.7 [1.6–1.9] and 1.56 [1.4–1.7], respectively, p = 0.02), and a higher cIMT in children whose mothers were on medication as compared to controls (0.48 [0.44–0.52] and 0.46 [0.44–0.50], respectively, p = 0.03).Conclusion:In utero exposure to uncontrolled maternal diabetes has an effect on the cardiovascular structure and function in children aged 2−5 years. However, future work requires long-term follow-up from fetal to adult life to assess these changes over the life course.


2009 ◽  
Vol 29 (8) ◽  
pp. 2129-2138 ◽  
Author(s):  
Per Svensson ◽  
Ingela Bergqvist ◽  
Stefan Norlin ◽  
Helena Edlund

ABSTRACT Notch signaling regulates pancreatic cell differentiation, and mutations of various Notch signaling components result in perturbed pancreas development. Members of the Fringe family of β1,3-N-acetylglucosaminyltransferases, Manic Fringe (MFng), Lunatic Fringe (LFng), and Radical Fringe (RFng), modulate Notch signaling, and MFng has been suggested to regulate pancreatic endocrine cell differentiation. We have characterized the expression of the three mouse Fringe genes in the developing mouse pancreas between embryonic days 9 and 14 and show that the expression of MFng colocalized with the proendocrine transcription factor Ngn3. In contrast, the expression of LFng colocalized with the exocrine marker Ptf1a, whereas RFng was not expressed. Moreover, we show that expression of MFng is lost in Ngn3 mutant mice, providing evidence that MFng is genetically downstream of Ngn3. Gain- and loss-of-function analyses of MFng by the generation of mice that overexpress MFng in early pancreatic progenitor cells and mice with a targeted deletion of MFng provide, however, evidence that MFng is dispensable for pancreas development and function, since no pancreatic defects in these mice were observed.


2015 ◽  
Vol 87 ◽  
pp. S131
Author(s):  
Neelu E Varghese ◽  
Gobinath Shanmugam ◽  
Daniel J Bolus ◽  
Balu K Chacko ◽  
Victor M Darley-Usmar ◽  
...  

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